Open AccessHTLV-1 activates YAP via NF-κB/p65 to promote oncogenesis
Author(s) -
Tiejun Zhao,
Zhilong Wang,
Jinyong Fang,
Wenzhao Cheng,
Shujun Zhang,
Jinhua Huang,
Lingling Xu,
Hongwei Gou,
LingHui Zeng,
Zhigang Jin,
Masao Matsuoka
Publication year - 2022
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.2115316119
Subject(s) - hippo signaling pathway , effector , microbiology and biotechnology , carcinogenesis , regulator , signal transduction , biology , cell growth , suppressor , yap1 , transcription factor , cancer research , genetics , gene
Significance The Hippo pathway plays critical roles in controlling cell proliferation, and its dysregulation is widely implicated in numerous human cancers. YAP, a Hippo signaling effector, often acts as a nexus and integrator for multiple prominent signaling networks. In this study, we discover NF-κB cross talk with the Hippo pathway and identify p65 as a critical regulator for YAP nuclear retention and transcriptional activity. Furthermore, we find that p65-induced YAP activation is essential for maintaining the proliferation of ATL cells in vitro and in vivo. Our findings unravel the functional interplay between NF-κB and YAP signaling and provide mechanistic insights into the YAP-dependent growth control pathway and tumorigenesis.